Iron deficiency (IDA) and chronic disease (ACD) anemia are complications of inflammatory bowel diseases (IBDs). Therapeutic modalities in remission and active IBD depend on the type of anemia. This study evaluated the link between hepcidin-25, proinflammatory cytokines, and platelet activation markers as biomarkers of anemia and inflammation in active IBD and remission. This prospective observational study included 62 patients with IBD (49 with ulcerative colitis and 13 with Crohn’s) and anemia. Patients were divided into Group I (no or minimal endoscopic signs of disease activity and IDA), Group II (moderate and major endoscopic signs of disease activity and mild ACD), and Control group (10 patients with IBD in remission, without anemia). We assessed the difference among groups in the levels of CRP, hemoglobin (Hgb), serum iron, ferritin, hepcidin-25, interleukins, TNF–α, IFN-γ, soluble CD40 ligand, and sP-selectin. Hepcidin-25 levels were significantly higher in Group II versus Group I (11.93 vs. 4.48 ng/mL, p < 0.001). Ferritin and CRP values showed similar patterns in IBD patients: significantly higher levels were observed in Group II (47.5 ng/mL and 13.68 mg/L) than in Group I (11.0 ng/mL and 3.39 mg/L) (p < 0.001). In Group II, hepcidin-25 was positively correlated with ferritin (ρ = 0.725, p < 0.001) and CRP (ρ = 0.502, p = 0.003). Ferritin was an independent variable influencing hepcidin-25 concentration in IBD patients, regardless of disease activity and severity of anemia. IBD hepcidin-25 best correlates with ferritin, and both parameters reflected inflammation extent and IBD activity.

Background/Aims: To evaluate the side effects of two antiplatelet agents - ticagrelor and eptifibatide - in mice with experimentally-induced inflammatory bowel disease. Methods and Material: This study was designed as a controlled, animal, drug safety investigation. C57Bl/6 mice were used to establish the ulcerative colitis model by exposure to dextran sulfate sodium (DSS), and divided into three experimental groups: eptifibatide-treated (150 µg/day intraperitoneally; n = 10), ticagrelol-treated (1 mg/day via gastric tube; n = 10), and DSS-control (plain drinking water; n = 10). An unmodeled non-DSS group served as the experimental control. Complete blood count was taken for all mice at baseline (day 0, treatment initiation) and after four days of treatment. On day 4, all animals were sacrificed for autopsy. The primary outcome measure was bleeding, and the secondary outcomes were change in platelet count, hemoglobin level, and hematocrit level. Results: Neither ticagrelor nor eptifibatide treatment produced a significant effect on DSS colitis mice for the safety parameters measured. Platelet count and hemoglobin and hematocrit levels were statistically similar between the three DSS groups and the non-DSS control group (P > 0.05). Autopsy found no evidence of recent bleeding in liver, spleen, central nervous system or serous cavities. Conclusion: The antiplatelet agents ticagrelor and eptifibatide were safe in DSS colitis mice, suggesting their potential in humans suffering from ulcerative colitis, and supporting future safety studies.

Background/Aim: Vitamin D insufficiency/deficiency is often present in patients with Type-2 diabetes mellitus and could present a risc factor for rapid progression of diabetic nephropathy and for higher incidence of cardiovascular events. The aim of this study was to examine the influence of vitamin D supplementation on proteinuria, cholesterol, triglycerides, C-reactive protein and haemoglobin A1c in patients with Type-2 diabetes mellitus and vitamin D insufficiency/deficiency. Methods: We included 90 patients with Type-2 diabetes mellitus and vitamin D insufficiency/deficiency in this prospective, cohort study. Patients are divided in 3 equal groups: 30 patients with normal proteinura, 30 with microproteinuria and 30 with macroproteinuria. Therapy included 6 months of supplementation with cholecalciferol drops: first 2 months with 20000 IU twice weekly, than if level of vitamin D was below normal we procedeed with same dose next 4 months. If the level of vitamin D was normal we proceeded with 5000 IU twice weekly. At the begining and at the end of the study we measured levels of urea, creatinine, fasting blood glucose, calcium, phosphorus, cholesterol, triglycerides, C-reactive protein, haemoglobin A1c, intact parathyroid hormone, 24-hour urine protein and creatinine clearance. Levels of calcium, phosphorus and vitamin D are also checked 2 months after beginning of therapy due to possible correction of cholecalciferol dose. Results: The lowest level of vitamin D before therapy is found in patients with macroproteinuria, while at the end of the study we found statistically significant higher level of vitamin D in all three groups. After 6 months of therapy we found statistically significant decrease of 24-hour urine protein, cholesterol, triglycerides, haemoglobin A1c in all three groups, and C-reactive protein in patients with normal proteinuria and microproteinuria. Statistically significant negative correlation between vitamin D and 24-hour urine protein, cholesterol and C-reactive protein was found in patients with macroproteinuria. Also, statistically significant negative correlation was found between vitamin D and haemoglobin A1c, in patients with normal proteinuria, vitamin D and C-reactive protein in patients with microproteinuria. Conclusion: High-dose cholecalciferol supplementation and its preventive use in patients with Type-2 diabetes mellitus (with or without proteinuria) decreases cholesterol, triglycerides, proteinuria, C-reactive protein, haemoglobin A1c.

Differential diagnosis of globus sensation in an otherwise asymptomatic patient should include hypopharyngeal fibrovascular polyp to avoid potentially fatal complications like airway compromise following regurgitation. We present a case of a 74-year-old man with a 13-cm long hypopharyngeal fibrovascular polyp with 9 months history of globus sensation. A narrow stalk of the giant polyp allowed endoscopic removal and complete resection with the CO₂ laser. Histopathological examination was conclusive for the fibrovascular polyp.

Introduction. Erdheim-Chester disease (ECD) is a rare non-Langerhans-cell histiocytosis. About 500 cases are published so far. It is multisystemic disease characterised by bilateral symmetric long bones sclerosis. Main histopathological finding is accumulation of big foamy histiocytes, immunohistochemically positive to CD68, and negative to S-100 and CD1a. There are no guidelines that reliably identify population that requires therapy, but symptomatic ECD, organ failure and central nervous system involvement re-quire treatment. Case report. We described a patient with a multisystemic form of ECD affecting long bones, the hypophysis, abdomen, and the peripheral nerves. Five years after initial symptoms ECD was suspected. Prednison was initiated, 60 mg once a day. After obtaining the diagnosis of ECD, interferon alpha 2A was introduced, but soon after stopped due to severe side effects. Considering that histiocytes were positive to platelet derived growth factor receptor alpha (PDGFR alpha) imatinib mesylate was started, but after two months stopped due to no clinical and radiological improvement. The disease was worsening and the patient died. Conclusion. We described the patient with intraperitoneal form of ECD, without cardiac and pulmonary involvement. There are several important issues: the diagnosis of ECD could be difficult to make, three treatment regimens were included and the patient died nine years after the initial symptoms due to indolent course of the disease and unsuccessful treatment.

Based on the role of platelets in inflammation and hemostasis it has been assumed that antiplatelet therapy could be beneficial for patients suffering from ulcerative colitis. Platelets present a link between inflammation and coagulation. They have more than 300 active mediators stored in their granules. Upon activation, platelet degranulate and release a lot of microparticles and mediators and interact with other immune and non-immune cells thereby amplifying inflammation. The most important parameters of platelet activation are P-selectin and CD40 ligand expressed on their surface upon activation, and their soluble forms presented in blood. Today, we have potent anti-platelet drugs that can inhibit platelet activation and degranulation, and thereby reduce inflammation. The most important drugs are P2Y12 receptor antagonists such as ticagrelor and clopidogrel and glycoprotein IIbIIIa inhibitors. Ticagrelor is an active drug and besides antiplatelet activity, it has bactericidal activity against Gram-positive strains and Clostridium difficile. Clopidogrel is a prodrug with less anti-inflammatory effect than ticagrelor and no proven bactericidal activity. Glycoprotein IIbIIIa inhibitors are very potent in reducing platelet aggregation but have lower anti-inflammatory potential than ticagrelor and clopidogrel.